# Exploring new rehabilitation pathways for stroke based on the comorbidity of post-stroke hypoesthesia with anxiety and depression

## TL;DR

This paper explores how post-stroke sensory loss and emotional disorders like anxiety and depression are linked, suggesting new rehabilitation approaches that address both together.

## Contribution

It proposes a novel bidirectional model linking sensory and emotional impairments after stroke, advocating for integrated rehabilitation strategies.

## Key findings

- Post-stroke hypoesthesia involves structural and functional brain changes that contribute to anxiety and depression.
- Emotional disorders like anxiety and depression further hinder sensory recovery and rehabilitation compliance.
- A sensory–emotional co-regulation rehabilitation approach is suggested for better outcomes in stroke patients.

## Abstract

Post-stroke hypoesthesia is a common yet often overlooked sequela, involving diminished capacities in touch, temperature, and pain perception. Recent studies suggest that sensory deficits not only hinder functional recovery but also show a high rate of comorbidity with anxiety and depression.

This study aims to systematically integrate the neural mechanisms, perceptual processing features, and behavioral consequences of post-stroke hypoesthesia and emotional disorders, to explore their comorbid relationship and propose more targeted rehabilitation strategies based on these mechanisms.

This review conducts an interdisciplinary literature search, integrating research from neuroimaging, cognitive neuroscience, and rehabilitation medicine, including 73 relevant studies. The keywords used in the screening are “Hypesthesia,” “Impaired Sensation,” “Anxiety,” and “Depression,” covering studies on sensory impairments and mood disorders. By comparing the sensory-emotion interaction mechanisms in stroke and non-stroke populations, a bidirectional model is constructed.

Findings indicate that post-stroke hypoesthesia results not only from structural damage in regions such as the thalamus, insula, and prefrontal cortex, but also from functional disruptions in perceptual processing. These impairments contribute to a closed-loop mechanism involving neural dysconnectivity and predictive coding dysfunction, which facilitates the emergence of anxiety and depression. In turn, these emotional disorders further suppress sensory recovery, significantly reducing patients’ motivation and rehabilitation compliance.

Post-stroke hypoesthesia should be recognized as a critical etiological and maintaining factor in anxiety and depression. The coexistence of pathological and functional mechanisms underscores the need for rehabilitation strategies that transcend the boundaries of perception, emotion, and cognition. Developing a rehabilitation pathway centered on “sensory–emotional co-regulation” can facilitate early identification, subtype-specific intervention, and comprehensive support for emotional comorbidities following stroke.